Disturbances in circulating opsonic activity in man after operative and blunt trauma

A humoral factor deficit (α-2-opsonic glycoprotein) important for reticuloendothelial (RE) phagocytosis has been previously identified in animals as a major etiologic mechanism for RE host defense failure following trauma or operation. Assessment of this opsonic factor in man during the 72-hr period following extensive multiple trauma ( n = 20) and major elective surgery ( n = 13) revealed a transient depression of this opsonic protein at 24-hr postinjury in both surgical patients and surviving multiple trauma patients. Recovery of normal opsonic activity occurred by 48–72 hr postinjury in both groups. Nonsurviving multiple trauma patients had very low levels of circulating opsonic activity with no tendency toward recovery. The influence of an overnight fast in both preoperative patients ( n = 8) and normal volunteers ( n = 9) did not adversely affect the level of this humoral factor. Recovery of normal opsonic activity occurred during the 72-hr postoperative period, a time of diminished calorie intake, suggesting that a brief nutritional deficit is not solely responsible for postoperative RE depression. Altered RE function in patients following multiple trauma and major elective surgery may have important consequences in terms of the intravascular clearance of blood-borne particulate material such as platelet aggregates, fibrin, microthrombi, and other potentially noxious substances.